Amyloid-β immunisation for Alzheimer's disease
Open accessAbstract
Alzheimer's disease is the main cause of dementia in elderly people and is becoming an ever greater problem as societies worldwide age. Treatments that stop or at least effectively modify disease course do not yet exist. In Alzheimer's disease, the conversion of the amyloid-beta peptide (Abeta) from a physiological water-soluble monomeric form into neurotoxic oligomeric and fibrillar forms rich in stable beta-sheet conformations is an important event. The most toxic forms of Abeta are thought to be oligomers, and dimers might be the smallest neurotoxic species. Numerous immunological approaches that prevent the conversion of the normal precursor protein into pathological forms or that accelerate clearance are in development. More than ten new approaches to active and passive immunotherapy are under investigation in clinical trials with the aim of producing safe methods for immunological therapy and prevention. A delicate balance between immunological clearance of an endogenous protein with acquired toxic properties and the induction of an autoimmune reaction must be found.
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Clinical trials have not provided definitive answers as to the direct role of AβPs or tangles in the cognitive impairment associated with AD pathologic diagnosis.
“In sum, clinical trials have not provided definitive answers as to the direct role of AβPs or tangles in the cognitive impairment associated with AD pathologic diagnosis (80, 81).”
From Correlation of Alzheimer Disease Neuropathologic Changes With Cognitive Status: A Review of the Literature (2012) · cites this paper as [80]
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References 91 · Cited by 155
- Authors
- Wisniewski, T., & Konietzko, U.
- Affiliations
- University of Zurich (CH)
- ORCID
- Konietzko, Uwe
- Venue
- The Lancet Neurology
- Publisher
- Elsevier BV
- Published
- 2008-09
- Volume
- 7
- Issue
- 9
- Pages
- 805-811
- ISSN
- 1474-4422 (ISSN-L)
- PMC
- PMC2752661
- OpenAlex
- W2115574704
- Cited by
- 155
- References
- 91
- Citations by year
- 2026: 2 · 2025: 5 · 2024: 4 · 2023: 4 · 2022: 7 · 2021: 6 · 2020: 7 · 2017: 5 · 2016: 7 · 2015: 5 · 2014: 8 · 2013: 7 · 2012: 15
- FWCI
- 2.64
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- The Lancet Neurology (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Zurich Open Repository and Archive (University of Zurich) (submittedVersion)
- Funders
- Schweizerischer Nationalfonds zur Förderung der Wissenschaftlichen Forschung (112616)
- National Institutes of Health
- National Institute on Aging (AG008051, AG15408, R01AG015408, AG20245, P30AG008051, R01AG020245)
- Topics
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Keywords
- Alzheimer's disease, amyloid-beta, immunization, active immunotherapy, passive immunotherapy, amyloid-beta oligomers, amyloid-beta dimers, β-sheet fibrils, autoimmunity, amyloid-beta clearance, clinical trials
- MeSH terms
- Alzheimer Disease, Animals, Brain, Humans, Immunization, Passive, Immunologic Factors, Protein Conformation, Amyloid beta-Peptides, Immunotherapy, Active, Alzheimer Vaccines, Mice, Plaque, Amyloid
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